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Mediators of Inflammation
Volume 2013 (2013), Article ID 495848, 8 pages
Research Article

IL-1β and IL-6 Upregulation in Children with H1N1 Influenza Virus Infection

1Department of Pediatrics, Catholic University of the Sacred Heart, A. Gemelli Hospital, Policlinico Gemelli, Largo Gemelli, 1-00168 Rome, Italy
2Pediatric Intensive Care Unit, Catholic University of the Sacred Heart, A. Gemelli Hospital, 00168 Rome, Italy

Received 22 June 2012; Accepted 31 March 2013

Academic Editor: Ger Rijkers

Copyright © 2013 Antonio Chiaretti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The role of cytokines in relation to clinical manifestations, disease severity, and outcome of children with H1N1 virus infection remains thus far unclear. The aim of this study was to evaluate interleukin IL-1β and IL-6 plasma expressions and their association with clinical findings, disease severity, and outcome of children with H1N1 infection. We prospectively evaluated 15 children with H1N1 virus infection and 15 controls with lower respiratory tract infections (LRTI). Interleukin plasma levels were measured using immunoenzymatic assays. Significantly higher levels of IL-1β and IL-6 were detected in all patients with H1N1 virus infection compared to controls. It is noteworthy to mention that in H1N1 patients with more severe clinical manifestations of disease IL-1β and IL-6 expressions were significantly upregulated compared to H1N1 patients with mild clinical manifestations. In particular, IL-6 was significantly correlated with specific clinical findings, such as severity of respiratory compromise and fever. No correlation was found between interleukin expression and final outcome. In conclusion, H1N1 virus infection induces an early and significant upregulation of both interleukins IL1β and IL-6 plasma expressions. The upregulation of these cytokines is likely to play a proinflammatory role in H1N1 virus infection and may contribute to airway inflammation and bronchial hyperreactivity in these patients.